When you pop a mint into your mouth, do you ever wonder what the molecular basis of the sensation of cold comes from? Probably not. But it is very important that a process of some kind should take place at all. Indeed, since the dawn of life, the minutest of organisms have needed some kind of mechanism with which they can make the difference between hot and cold – be it simply to avoid the one or the other under extreme conditions. It is all a question of survival.

Humans – like all living organisms – are provided with hosts of sensory cells. Not so long ago, it was discovered that what made the cells sensory were a series of channels known as the TRP channels, or the Transient Receptor Potential channels. These are transmembrane channels which are voltage-gate dependent and are probably activated via receptors. What happens is that when a ligand binds to its receptor, this would cause the TRP channel to open – or close – thus modifying the ion flow across the cell membrane. In this way, a message – cold or hot, sweet or sour – is transmitted from the tip of a sensory cell to our brain where it is processed and consequently acted upon.

TPR channels are scattered throughout the whole of the animal kingdom. Nematodes use them as noses to detect noxious chemicals, mice use them in pheromone-sensing to distinguish males from females, and humans use them for the purpose of tasting and discriminating warmth. In this respect, one particular TPR channel – TPRPM8 – was found to be at the heart of our sensation of cold. The definition of ‘cold’ is defined as temperatures between 8 and 28 degrees Celsius. What some could call hot… How TPRPM8 functions is not known in detail, yet one interesting find was that menthol enhanced its activation.

Does this mean that we should beat a hasty retreat when faced with a mint? No. But what it does suggest is that the hypothesis that TRP channels are stimulated via ligands – in this case, menthol – may well be valid.